• Journal of Yeungnam Medical Science
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• v.38 no.1
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• pp.70-73
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• 2021

Relapsing polychondritis (RP) is a rare, progressive immune-mediated systemic inflammatory disease of unknown etiology, characterized by recurrent inflammation of cartilaginous structures. Approximately 30% of RP cases are associated with other autoimmune diseases. However, the co-occurrence of RP and Crohn disease (CD) has rarely been reported. Herein, we present a 35-year-old woman diagnosed with RP and CD, who was refractory to initial conventional medications, including azathioprine and glucocorticoid, but who subsequently responded to infliximab (IFX). For both diseases, remission was sustained with IFX. There has been no previous report regarding the successful treatment of co-existing RP and CD with IFX.

• Biomolecules & Therapeutics
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• v.30 no.5
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• pp.409-417
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• 2022

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide, and accumulating evidence indicates that mitochondrial dysfunction is associated with progressive deterioration in PD patients. Previous studies have shown that sinapic acid has a neuroprotective effect, but its mechanisms of action remain unclear. The neuroprotective effect of sinapic acid was assayed in a PD mouse model generated by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) as well as in SH-SY5Y cells. Target protein expression was detected by western blotting. Sinapic acid treatment attenuated the behavioral defects and loss of dopaminergic neurons in the PD models. Sinapic acid also improved mitochondrial function in the PD models. MPTP treatment increased the abundance of mitochondrial fission proteins such as dynamin-related protein 1 (Drp1) and phospho-Drp1 Ser616. In addition, MPTP decreased the expression of the REV-ERB α protein. These changes were attenuated by sinapic acid treatment. We used the pharmacological REV-ERB α inhibitor SR8278 to confirmation of protective effect of sinapic acid. Treatment of SR8278 with sinapic acid reversed the protein expression of phospho-Drp1 Ser616 and REV-ERB α on MPTP-treated mice. Our findings demonstrated that sinapic acid protects against MPTP-induced PD and these effects might be related to the inhibiting abnormal mitochondrial fission through REV-ERB α.

• Tuberculosis and Respiratory Diseases
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• v.87 no.1
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• pp.40-51
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• 2024

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial pneumonia with a very poor prognosis. Accurate diagnosis of IPF is essential for good outcomes but remains a major medical challenge due to variability in clinical presentation and the shortcomings of existing diagnostic tests. Medical history collection is the first and most important step in the IPF diagnosis process; the clinical probability of IPF is high if the suspected patient is 60 years or older, male, and has a history of cigarette smoking. Systemic assessment for connective tissue disease is essential in the initial evaluation of patients with suspected IPF to identify potential causes of interstitial lung disease (ILD). Radiologic examination using high-resolution computed tomography plays a pivotal role in the evaluation of patients with ILD, and prone and expiratory computed tomography images can be considered. If additional tests such as surgical lung biopsy or transbronchial lung cryobiopsy are needed, transbronchial lung cryobiopsy should be considered as an alternative to surgical lung biopsy in medical centers with experience performing this procedure. Diagnosis through multidisciplinary discussion (MDD) is strongly recommended as MDD has become the cornerstone for diagnosis of IPF, and the scope of MDD has expanded to monitoring of disease progression and suggestion of appropriate treatment options.

• Journal of Korean Physical Therapy Science
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• v.9 no.2
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• pp.159-170
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• 2002

Parkinson's disease(PD) is a progressive neurodegenerative disease that affects the functioning of the basal ganglia, a brain area that contributes to the control of movement. The disease is caused by the death of nerve cells in the brain that produce dopamine, a chemical messenger. The cells affected usually produce a neurotransmitter(a chemical that transmits nerver impulses) called dopamine, which acts with acetylcholine, another neurotransmitter, to fine-tune muscle control. In Parkinson's disease, the level of dopamine relative to acetylcholine is reduced, adversely affecting muscle control. When the supply of dopamine is depleted, the function of the basal ganglia is disrupted and its ability to control movement-deteriorates. The result is that PD patients experience moderate rigidity, difficulty in initiating movements and slowness in executing them, and a rhythmical tremor at rest. Although the cause of Parkinson's disease is not known, genetic factors may be involved. About 3 in 10 people with the disorder have an affected family member. About 1 in 100 people over the age of 60 in the US have Parkinson's disease. And Parkinson's disease is slightly more common in men. The course of the disease is variable, but drags may be the best effective in treating the symptoms and improving quality of life. But, The doctor may arrange physical therapy to help with physical mobility problems. It is important to continue to exercise and take care of your general health. Try to take a walk each day. Stretching exercises can help you maintain your strength and mobility. So, This papers will serve about the information of PD for clinical physical therapist. Finally, The aim of review is increasing approach method and technique for PD patients by the view of physical therapy.

• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.8 no.2
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• pp.73-87
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• 2002

Parkinson's disease(PD) is a progressive neurodegenerative disease that affects the functioning of the basal ganglia, a brain area that contributes to the control of movement. The disease is caused by the death of nerve cells in the brain that produce dopamine, a chemical messenger. The cells affected usually produce a neurotransmitter(a chemical that transmits nerver impulses) called dopamine, which acts with acetylcholine, another neurotransmitter, to fine-tune muscle control. In Parkinson's disease, the level of dopamine relative to acetylcholine is reduced, adversely affecting muscle control. When the supply of dopamine is depleted, the function of the basal ganglia is disrupted and its ability to control movement deteriorates. The result is that PD patients experience moderate rigidity, difficulty in initiating movements and slowness in executing them, and a rhythmical tremor at rest. Although the cause of Parkinson's disease is not known, genetic factors may be involved. About 3 in 10 people with the disorder have an affected family member. About 1 in 100 people over the age of 60 in the US have Parkinson's disease. And Parkinson's disease is slightly more common in men. The course of the disease is variable, but drugs may be the best effective in treating the symptoms and improving quality of life. But, The doctor may arrange physical therapy to help with physical mobility problems. It is important to continue to exercise and take care of your general health. Try to take a walk each day. Stretching exercises can help you maintain your strength and mobility. So, This papers will serve about the information of PD for clinical physical therapist. Finally, The aim of review is increasing approach method and technique for PD patients by the view of physical therapy.

• The Journal of Internal Korean Medicine
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• v.18 no.2
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• pp.177-194
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• 1997

This thesis, deduced from studying eastern and western medical records, deals with geriatric demedtia in modern society. The result were obtained as follows : 1. Dementia is a kind of chronic, progressive, degenerative disease. The chief expression and pathogenic change of the disease is organic: e.g., extensive change such as cerebrum - atrophy, and denaturalization result. in such a situation intellectual capacities and the ability to enjoy daily life deteriorate trenendously. 2. A basic internal cause of the disease is Defficiencies of the heart, liver and kidneys. An exterior cause is an Excessiveness of the 'Dam'(痰), 'Blood Stasis', 'Fung'(風) and 'Fire'. In a Western Medical view, the reason for dementia is due to the onset of Alzheimer's disease and Brain anemia resulting from Multi - infarction or some other reason. If the white - matter of the brain is injured, then dementia easily to results. 3. Disease symptoms result in troubles in intellectual functions : e.g., memory, orientation, intelligence, judgement, common sence and calculating abilities. 4. The proper therapeutic treatment depends on the causes. When the Deficiency is serious, Fortification (heart, liver. and kidney deficiency) is applied and Decrease is follow. When Excessiveness of wrong is serious, the Decrease is tried before the supplement measure is used depending on the deficiency, which generally is used together with 'Fortify Right - Decreace Wrong'. 5. If the disease wasn't caused by some mental reason, it's difficult to be cured of the disease. When the degree of the disease is light and it doesn't continue for a long time, the therapeutic treatment can block the disease's progress and improve the patient's symptoms.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.12 no.1
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• pp.42-48
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• 2012

Pompe disease is a rare lysosomal glycogen storage disorder caused by a total or partial deficiency of the acid ${\alpha}$-glucosidase (GAA) enzyme due to the GAA gene mutations. The classic infantile form of Pompe disease is a rapidly progressive multi-organ disease with hypotonia, generalized muscle weakness, and hypertrophic cardiomyopathy, usually leading to death in the first 2 years of life. Enzyme replacement therapy with recombinant human GAA has been shown to be effective and subsequently yielded promising results. Here, we present clinical and genetic characteristics of three Korean non-classic infantile Pompe patients, and the short term efficacy of enzyme replacement therapy. Considering that enzyme replacement therapy can change the natural course of infantile Pompe disease, early diagnosis and early initiation of treatment is critical to improving patient outcomes.

• The Journal of the Korean dental association
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• v.11 no.10
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• pp.643-647
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• 1973

The auther has made the oral examination of 523 pregnant women-such as calculus, gingival disease, periodontal disease, and dental caries-who visit the dental department and obstetric department in National Medical Center in Seoul. After the above studies, results of the changes of the pregnant women's oral condition are following. 1. In creasing of calculus deposition due to the changes of saliva components. 2. Increasing of incidence of gingival and periodontal and pathological changes followed by calculus deposition. 3. Incidence of new cavities are not related to the pregnancy, but old cavities have become more progressive in dental caries.

• Annals of Clinical Neurophysiology
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• v.14 no.1
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• pp.36-40
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• 2012

Nephrogenic systemic fibrosis (NSF) is a systemic disease that affects the skin and other tissues in patients with renal insufficiency and exposure to gadolinium-containing contrast. A 55-year-old woman with end-stage renal disease on hemodialysis was consulted for progressive general weakness. After she had undergone multiple MRIs with gadolinium-containing contrast media, muscle weakness and skin lesions were developed. Her skin and muscle biopsy specimens showed CD34+ fibroblast entrapping collagen bundles. There are few reports of NSF with myopathy.

• Journal of Interdisciplinary Genomics
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• v.2 no.2
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• pp.20-25
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• 2020

Mucopolysaccharidosis type III (MPS III or Sanfilippo syndrome) is a multisystem lysosomal storage disease that is inherited in an autosomal recessive manner. It consists of four subtypes (MPS IIIA, B, C, and D), each characterized by the deficiency of different enzymes that catalyze the metabolism of the glycosaminoglycan heparan sulfate at the lysosomal level. The typical clinical manifestation of MPS III includes progressive central nervous system (CNS) degeneration with accompanying systemic manifestations. Disease onset is typically before the age of ten years and death usually occurs in the second or third decade due to neurological regression or respiratory tract infections. However, there is currently no treatment for CNS symptoms in patients with MPS III. Invasive and non-invasive techniques that allow drugs to pass through the blood brain barrier and reach the CNS are being tested and have proven effective. In addition, the application of genistein treatment as a substrate reduction therapy is in progress.